Hearing loss or impairment is a common occurrence for mammals. Impairment anywhere along the auditory pathway from the external auditory canal to the central nervous system may result in hearing loss. Auditory apparatus can be divided into the external and middle ear, inner ear and auditory nerve and central auditory pathways. While having some variations from species to species, the general characterization is common for all mammals.
Auditory stimuli are mechanically transmitted through the external auditory canal, tympanic membrane, and ossicular chain to the inner ear. The middle ear and mastoid process are normally filled with air. Disorders of the external and middle ear usually produce a conductive hearing loss by interfering with this mechanical transmission. Common causes of a conductive hearing loss include obstruction of the external auditory canal, as can be caused by aural atresia or cerumen; thickening or perforation of the tympanic membrane, as can be caused by trauma or infection; fixation or resorption of the components of the ossicular chain; and obstruction of the Eustachian tube, resulting in a fluid-filled middle-ear space.
Auditory information is transduced from a mechanical signal to a neurally conducted electrical impulse by the action of neuro-epithelial cells (hair cells) and first-order neurons (spiral-ganglion cells) in the inner ear. All central fibers of spiral-ganglion cells form synapses in the cochlear nucleus of the pontine brain stem. The auditory projections from the cochlear nucleus are bilateral, with major nuclei located in the inferior colliculus, medial geniculate body of the thalamus, and auditory cortex of the temporal lobe. Although the details of the neurophysiology of the inner ear and central auditory projections are beyond the scope of this review, a few specific observations are important for an understanding of the localization of hearing loss. First, the number of neurons involved in hearing increases dramatically from the cochlea to the auditory brain stem and the auditory cortex. All auditory information is transduced by a limited number of hair cells, of which the so-called inner hair cells, numbering a comparative few, are critically important, since they form synapses with approximately 90 percent of the primary auditory neurons. By comparison, at the level of the cochlear nucleus, the number of neural elements involved is measured in the hundreds of thousands. Thus, damage to a relatively few cells in the auditory periphery can lead to substantial hearing loss. Hence, many causes of sensorineural loss can be ascribed to lesions in the inner ear. This hearing loss can be progressive and is irreversible.
The hearing of pet animals, like that of humans, becomes significantly less acute because of changes in the anatomy of the ear as the animal ages. The anatomic basis for hearing loss in pet animals has received little attention. When hearing loss such as that herein-described occurs, the sum total of physiological events that occur is perceived by those observing the animal as inadequate behavioral response to sounds such as commands.
Of course, proper function of the individual components of the auditory system is important for pet owners to maximize the enjoyment of their pet. Like humans, pet animals that cannot hear do not adequately respond to environmental stimuli. Thus, the animal is often perceived as slow, "dumb", and not as fun as in its youth, when the true cause for these human perceptions is simply hearing impairment.
Use of mechanical hearing aids for animals is simply not practical for obvious reasons. There is, therefore, a need to treat hearing loss in animals such as dogs, cats, horses and other pets. This invention has as its primary objective the fulfillment of this continuing need.
Selegiline is a selective monoamine oxidase B (MAO-B) inhibitor, which is widely used as an adjunct in the treatment of Parkinson's disease. While its most common usage is for the treatment of Parkinson's disease, selegiline was originally developed as an antidepressant agent. Recent testing has indicated that selegiline may have some effect on increasing sexual response in aging animals, and also may have some effect, at least in rats, in increasing the natural life span. However, to date selegiline has only been medically approved by regulatory agencies for use for treatment of Parkinson's disease.
Like most drugs, selegiline can have diverse physiological effects which are completely dependent upon the dose administered. In accordance with the present invention, selegiline can be used for successful methods of treatment to provide the desired physiological effects enumerated herein, providing that it is used at the dosage levels mentioned herein, and providing it is administered at the periodic intervals and for the time spans mentioned herein. Obviously, when different dosages and levels of treatment are used, the results expressed herein may not be achieved. In fact, at higher doses adverse behavioral effects may be encountered.